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Applied Clinical Veterinary Nursing > Neuromuscular Blocking Agents > Flashcards

Neuromuscular Blocking Agents Flashcards

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1
Q

which classes of drugs provide muscle relaxation?

A

local anaesthetics
benzodiazepines
a2-adrenoreceptor agonists
guaiphenesin
neuromuscular blocking agents

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2
Q

why does ketamine require an adjunct muscle relaxant?

A

ketamine alone causes muscle rigidity

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3
Q

what is guaiphenesin?

A

a centrally acting muscle relaxant

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4
Q

where does guaiphenesin act?

A

internuncial neurones of spinal cord, brainstem and subcortical areas of brain

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5
Q

does guaiphenesin have analgesic/anaesthetic properties?

A

no

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6
Q

what effect does guaiphenesin have on the blood?

A

induces haemolysis if given at concentrations over 10%

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7
Q

which concentration of guaiphenesin induces haemolysis?

A

> 10%

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8
Q

what happens if guaiphenesin is given at concentrations over 10%?

A

causes haemolysis

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9
Q

how should guaiphenesin be administered?

A

slow IV only

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10
Q

why should guaiphenesin only be given IV?

A

causes tissue damage if goes perivascular

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11
Q

when is guaiphenesin typically given?

A

infused during induction of anaesthesia to reduce rigidity effects of ketamine

can be used in triple anaesthetic protocol in horses

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12
Q

what are the clinical indications for use of NMBAs?

A

relaxation of skeletal muscles for surgical access

facilitate control of ventilation

facilitate tracheal intubation in cats and pigs

ophthalmic surgery

assist reduction of dislocated joints and fractures

reduction in amount of anaesthetic required

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13
Q

how can NMBAs help with thoracic/abdominal surgery?

A

can help facilitate retraction in deep abdominal/thoracic surgery

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14
Q

how do NMBAs facilitate control of ventilation?

A

paralysis of respiratory muscles in order control ventilation more easily

ventilation during thoracotomy

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15
Q

when can NMBAs be useful in reduction of dislocated joints/fractures?

A

only if injury is recent - less success with longstanding injury

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16
Q

how may use of NMBAs help reduce amount of anaesthetic required?

A

aids muscles relaxation so that inhalant/injectable can be reduced

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17
Q

what separates the motor neurone and muscle cell?

A

synaptic cleft

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18
Q

what is separated by the synaptic cleft?

A

motor neurone and muscle cell

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19
Q

what is released from the nerve endings when a signal is recieved?

A

acetylcholine

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20
Q

when/where is acetylcholine released?

A

from the nerve endings when a signal is received

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21
Q

where does acetylcholine bind?

A

to the post-synaptic nicotinic receptor

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22
Q

how many acetylcholine subunits must be bound to the post-synaptic nicotinic receptor?

A

two

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23
Q

what does binding of the acetylcholine to the receptors result in?

A

muscle contraction

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24
Q

how is muscle contraction achieved?

A

binding of 2 Ach subunits to the post-synaptic nicotinic receptor

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25
Q

what breaks down acetylcholine?

A

rapidly hydrolysed by acetylcholinesterase within the synaptic cleft

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26
Q

why is muscle contraction short-lived?

A

ACh is rapidly hydrolysed by acetylcholinesterase

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27
Q

what does acetylcholinesterase do?

A

hydrolyses acetylcholine

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28
Q

what is very important to remember when considering NMBDs as part of an anaesthetic regimen?

A

they have no analgesic or anaesthetic effects

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29
Q

what facilities are important to prepare when using NMBDs?

A

facilities for ET intubation and IPPV

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30
Q

which parts of the body are most and least sensitive to NMBDs?

A

most effect peripherally and least centrally (diaphragm and intercostals most resistant)

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31
Q

what are depolarising muscle relaxants?

A

ACh receptor agonists

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32
Q

how do depolarising muscle relaxants work?

A

They bind to Ach receptors and generate an action potential, but are not metabolised by acetylcholinesterase so they result in extended depolarisation of the muscle end plate (cannot repolarise)

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33
Q

what is the most common depolarising muscle relaxant?

A

suxamethonium

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34
Q

how is suxamethonium broken down?

A

by pseudocholinesterase/plasma cholinesterase

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35
Q

what is the onset of suxamethonium?

A

rapid - 2-3 mins

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36
Q

why is an initial muscle fasciculation seen with depolarising muscle relaxants?

A

they function by generating a (prolonged) action potential to depolarise the muscle cells

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37
Q

how many doses of suxamethonium can be given?

A

one

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38
Q

what happens after more than one dose of suxamethonium is given?

A

phase II block

39
Q

what is the duration of action of suxamethonium?

A

3-5 mins in cats
20 mins in dogs

40
Q

in which species can suxamethonium aid intubation?

A

cats and pigs

41
Q

what is usually combined with thiopental during induction of anaesthesia for muscle relaxation in horses?

A

suxamethonium

42
Q

what might suxamethonium do to body temperature?

A

may trigger malignant hypothermia

43
Q

how does suxamethonium affect serum potassium levels?

A

increases

44
Q

why should care be taken using suxamethonium in those with UT issues or CVS instability?

A

suxamethonium increases serum potassium levels

45
Q

what is immediate side effect of suxamethonium injection

A

it burns

46
Q

what are non-depolarising muscle relaxants also called?

A

competitive muscle relaxants

47
Q

how do non-depolarising muscle relaxants work?

A

they compete with Ach for post-junctional binding sites

48
Q

why is there no initial muscle fasciculation with non-depolarising muscle relaxants?

A

they do not generate an action potential

49
Q

what is the speed of onset of non-depolarising muscle relaxants?

A

relatively slow

50
Q

can non-depolarising muscle relaxants be topped up?

A

yes

51
Q

how much can non-depolarising muscle relaxants be topped up by?

A

1/3rd of initial dose

52
Q

can non-depolarising muscle relaxants be antagonised?

A

yes

53
Q

how can non-depolarising muscle relaxants be used for maintained muscle relaxation?

A

via infusion

54
Q

what are the 2 most common non-depolarising muscle relaxants?

A

atracurium and vecuronium

55
Q

what is atracurium?

A

a non-depolarising muscle relaxant

56
Q

what is vecuronium?

A

a non-depolarising muscle relaxant

57
Q

how many active isomers are there in atracurium?

A

1 of a mixture of 10 isomers

58
Q

what is the active isomer of atracurium called?

A

cisatracurium

59
Q

how is atracurium eliminated?

A

hoffman elimination

60
Q

what is hoffman elimination?

A

a temperature-dependent reaction in plasma which eliminates atracurium

61
Q

what is eliminated by hoffman elimination?

A

atracurium

62
Q

why is atracurium the agent of choice for animals with renal/hepatic compromise

A

undergoes hoffman elimination in plasma rather than breakdown by liver/kidneys

63
Q

which muscle relaxant is the agent of choice for animals with renal/hepatic compromise?

A

atracurium

64
Q

why should atracurium be given slowly IV?

A

to avoid histamine release

65
Q

when is laudanosine produced?

A

can be produced by atracurium metabolism

66
Q

what can laudanosine produce?

A

can produce neurological effects - unlikely at clinical doses

67
Q

where should atracurium be stored?

A

in the fridge

68
Q

what is produced by metabolism of atracurium?

A

laudanosine

69
Q

what type of molecule is vecuronium?

A

a steroid compound (no corticosteroid effects)

70
Q

which non-depolarising muscle relaxant is a steroid compound?

A

vecuronium

71
Q

how slowly should vecuronium be administered?

A

no histamine release - speed of injection less important

72
Q

how much of a vecuronium dose undergoes hepatic biotransformation?

A

40-50%

73
Q

what form does vecuronium come in?

A

powder which needs reconstituting

74
Q

how long is vecuronium stable once reconstituted?

A

24 hours

75
Q

does vecuronium need to be stored in the fridge?

A

no

76
Q

what respiratory parameters are important to monitor when using NMBDs?

A

ventilation
check tube not kinked/dislodged
ensure breathing system connected
monitor movement of thoracic wall, ETCO2 and SpO2

77
Q

what are the signs of inadequate depth of anaesthesia while using a NMBD?

A

increase in pulse rate and blood pressure

salivation/lacrimation

vasovagal response

Increase in ETCO2

slight muscle twitching

pupillary dilation

78
Q

what can be observed in the vagovagal response?

A

bradycardia
hypotension
pallor

79
Q

which nerves can be used with a peripheral nerve stimulator?

A

ulnar
peroneal
facial

80
Q

what is the train of 4?

A

where 4 electrical impulses are applied to the nerve over a 2 second period to assess degree of neuromuscular blockade

81
Q

can the train of 4 be used to assess anaesthetic depth?

A

no

82
Q

which factors affect duration of the neuromuscular blockade?

A

dose administered

volatile agent

hypothermia (prolongs)

hepatic/renal insufficiency (prolongs)

electrolyte and acid-base abnormalities

muscle diseases (e.g. myasthenia gravis)

aminoglycoside abs (prolongs)

83
Q

what effect do muscle diseases (e.g. myasthenia gravis) have on neuromuscular blocking?

A

they greatly potentiate effect of the NMB agent - care with dose!

84
Q

how long do normal clinical doses of NMBDs last?

A

20-30 mins

85
Q

what are the main anticholinesterases called?

A

neostigmine and edrophonium

86
Q

what does acetylcholinesterase do?

A

breaks down acetylcholine

87
Q

what do anticholinesterases do?

A

interfere with the action of acetylcholinesterases

88
Q

how do anticholinesterases antagonise non-depolarising NMBs?

A

interfere with action of acetylcholinesterases - less is broken down so Ach concentration increases and competes with NMB agent for post-synaptic receptor

89
Q

what unwanted side-effects may be seen with use of antocholinesterases?

A

bradycardia
salivation
bronchospasm
diarrhoea

90
Q

which anticholinergic drugs are administered with anticholinesterase?

A

atropine or glycopyrrolate

91
Q

when can supported ventilation be ceased when using NMBDs?

A

when spontaneous ventilation returns

92
Q

what should be closely monitored on recovery when patients have had a NMBD?

A

URT weakness on recovery - swallowing reflex but then return of paralysis
URT sounds
cyanosis
paradoxical ventilation
inadequate respiratory effort

93
Q

why are anticholinergic agents given if antagonising non-depolarising muscle relaxants?

A

to lessen bradycardic effects

94
Q
A

Applied Clinical Veterinary Nursing (31 decks)

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